CV Physiology 4-6 Flashcards
In a normal heart, which ECG leads should have a positive (upwardly deflecting) T wave vs negative (downward deflecting) T wave? Why?
leads with positive QRS should have positive T wave: I, II, aVF
leads with negative QRS should have negative T wave: aVR
*remember that waves are positive when either depolarization is moving towards the positive lead, or repolarization is moving away from the positive lead
[QRS is ventricle depolarization, T wave is ventricle repolarization]
left axis deviation (LAD) vs right axis deviation (RAD) of cardiac electrical activity
normal cardiac electrical axis (direction in which most depolarization is headed) is between 0 (3pm) and 90 (6pm) degrees (towards the left ventricle)
LAD (left axis deviation): -30 (where aVL is) to -90 degrees
RAD (right axis deviation): >100 degrees
basically this means depolarization in the heart is not moving/spreading in the direction it is supposed to be
the positivity/negativity of which ECG leads define left axis deviation (LAD)?
LAD: cardiac electrical axis between -30 (2pm) to -90 (12pm)
defined by:
- positive lead I (0 degrees)
- negative lead II (60 degrees)
- negative aVF lead (90 degrees)
the positivity/negativity of which ECG leads define right axis deviation (RAD)?
RAD: cardiac electrical axis >100 degrees
defined by:
- negative lead I (0 degrees)
- positive aVF (90 degrees)
- positive lead III (120 degrees)
You’re reading a patient’s ECG and notice that lead I and aVL are positive, but aVF if negative.
What kind of deviation is this?
normal cardiac electrical axis has positive lead I and aVF
left axis deviation (between -30 to -90) has positive lead 1, negative aVF, and positive aVL
right axis deviation (>100 degrees) has negative lead I, positive aVF, and positive lead III
this patient has LAD
You’re reading a patient’s ECG and notice that lead I is negative, but aVF and lead III are positive.
What kind of deviation is this?
normal cardiac electrical axis has positive lead I and aVF
left axis deviation (between -30 to -90) has positive lead 1, negative aVF, and positive aVL
right axis deviation (>100 degrees) has negative lead I, positive aVF, and positive lead III
this patient has RAD
what are the two phases of the P wave of an ECG?
first half is right atrial depolarization, second half is left atrial depolarization
what does the P-R interval represent on an ECG?
PR interval = atrial to ventricular relay (AV nodal delay)
what does an abnormally wide/long QRS complex represent (electrically speaking)?
normal QRS is narrow/sharp
abnormally long QRS represents depolarization outside of the fast conducting path or defect in fast conducting path
[fast conducting path = bundle branches, Purkinje fibers]
use the anatomy of the heart to explain why it makes sense that P waves is biphasic on ECG at lead V1
P wave is actually 2 phases: first half is right atrial depolarization, second half is left atrial depolarization
anatomically, the left atrium sits posterior to the right atrium, so from a frontal plane they overlap
V1 is perpendicular to the flow of electrical current through the atrium - therefore P wave appears biphasic
establishment of what prevents retrograde conduction (reentry) in the heart?
establishment of effective refractory period keeps spread of action potential (depolarization) unidirectional
established via time and voltage dependent activation and inactivation
what is atrial flutter and how does it appear on ECG?
atrial flutter: rapid but regular atrial activity, can be caused by reentry
ECG - rapid atrial activity, profound P waves (saw-tooth appearance), T waves are masked by frequency of P waves
AV delay impedes relay of all atrial impulses during flutter, so ventricular rate depends on delay of AV delay
primary vs secondary vs tertiary heart block
how do each of these appear on ECG?
heart block = malfunction in AV node
primary: prolonged conduction time within AV node and/or bundle of His —> prolonged P-R interval
secondary: increased refractory period of AV node and/or bundle of His (less excitable), not every impulse is relayed through so there are more P waves than QRS complex
tertiary (complete heart block/AV dissociation): no atrial impulses reach ventricles, block can occur within AV node or beyond (worse more distally), pacemakers produce slower escape rhythm while atria beats independently at normal 60-100bpm —> multiple P waves superimposing on QRS complex
Mobitz I vs Mobitz II heart block
secondary heart block: increased refractory period of AV node or Bundle of His, making it less excitable —> more P waves than QRS complex, 2 forms:
Mobitz I: progressive prolongation of P-R until eventually a non-conducted P wave (dropped QRS)
Mobitz II: conduction block is below AV node (in bundle of His or bundle branches), P-R intervals do not alter prior to non-conducted P wave (dropped QRS)
explain why it is worse to have a tertiary heart block distal to the AV node
tertiary heart block = complete heart block = AV dissociation: no atrial impulses reach ventricles
if block is within AV node, pacemaker function at AV junction can produce junctional escape rhythm ~50bpm
blocks distal to AV node can only produce ventricular escape rhythm ~30-40bpm, while atria continues to beat at 60-100bpm - very unstable
describe atrial fibrillation (A fib) and how it appears on ECG
A fib: most common cardiac arrhythmia disorder, caused by disruption of sequence of electrical conduction —> formation of self-sustained electrical circuits which each rapidly depolarize only small islets of atrial myocardium —> chaotic reentry (reexcitation)
this disrupts AV nodal conduction and subsequently ventricular rhythm (—> supraventricular arrhythymia/tachycardia)
ECG - no P wave, fibrillatory waves (nonuniform) - irregularly irregular!
what is meant by cardiac reentry
reentry: abnormal electrical re-excitation of a region of myocardium that was previously excited (depolarization moving in the wrong direction)
what are the stages/classifications of atrial fibrillation (A fib)
recurrent: random episodes of A fib self-terminate
paroxysmal: recurring A fib episodes that occur after sinus rhythm is spontaneously restored following recurrent A fib
persistent: paroxysmal episode which does not spontaneously end (requires medical intervention to restore normal sinus rhythm)
permanent: not resolved by medical intervention
explain why patients with A fib experience episodes of postural lightheadedness
what is the serious risk associated with A fib?
A fib causes loss of atrial contribution to CO (~20%), which is by itself not a serious problem in an otherwise healthy person
compensation via tachycardia reduces ventricular filling time, lowering CO —> postural lightheadedness
serious risk associated with A fib is development of atrial thrombus —> systemic arterial embolism —> pulmonic embolism or ischemic stroke
describe ventricular fibrillation
v fib: wide-spread irregular contractions (fibrillations) of ventricular myocardium, can results from hypoxic ischemia/electrocution/drugs, rapidly fatal if not treated
initiated by ventricular tachycardia from multiple reentry wavelets - myocytes stimulated during vulnerable period during down-slope of T wave (end of repolarization) when there is extreme variability in excitability of myocytes (some populations re-stimulated, others not)
requires defibrillation with electrical current to cause uniform refraction so that SA node can regain control
describe bundle branch block and how this appears (generally) on ECG
BBB: delay/block in conduction within R/L branch of bundle of His —> impulses must be relayed from unaffected side via IV septum, through slower myocyte-myocyte conduction —> delay in conduction
ECG - in general, widened QRS
how do premature ventricular contractions (PVC) appear on ECG?
PVC: episodes of uncoordinated ventricular depolarization, commonly isolated
because PVC are ventricular in origin, ECG shows no P wave associated with aberrant QRS complex
how does myocardial infarction appear on ECG? (3 things)
infarct = area of necrosis which develops from sudden ischemia
MI ECG:
1. peaked T waves (repolarization) which invert a few hours later (represent ischemia, not specific for MI)
2. elevated ST segment (indicates myocardial injury) which normalizes several hours later
3. development of new Q waves (indicates irreversible myocardial death, represents misdirection of current away from dead region) - do not resolve
which electrical leads would indicate occlusion of the right coronary artery on ECG?
right coronary artery: supplies inferior and posterior regions of heart
occlusion (causing infarction) would be indicated by electrical activity of inferior leads: II, III, aVF
posterior heart does not have dedicated lead, so would rely on reciprocal changes evident by lead V1
which electrical leads would indicate occlusion of the left circumflex artery on ECG?
occlusion of left circumflex artery would cause infarction of left lateral myocardium - visualize with left lateral ECG leads: I, aVL, V5, V6
which electrical leads would indicate occlusion of the left anteriorly descending artery on ECG?
LAD supplies anterior myocardium
occlusion would be indicated by the precordial (anterior) leads V1-V6
describe physiologic splitting of the S2 heart sound occurs on inspiration
S2 = closure of semilunar valves, actually split into aortic (A2) and pulmonic (P2) valve component
inspiration decreases intrathoracic pressure, which allows:
1. increased capacitance of pulmonary arteries and veins which reduces reduces diastolic back pressure against pulmonic valve, alleviating driving force to close pulmonic valve such that it closes later
2. decreased pulmonary vein pressure which reduces left heart diastolic filling, reducing time for systole —> aortic valve closure occurs sooner
widened vs paradoxical splitting of S2
S2 = closure of semilunar valves, actually split into aortic (A2) and pulmonic (P2) valve component
widened splitting: increase in delay between A2 and P2 due to delayed pulmonic valve closure (right bundle branch block or pulmonic valve stenosis)
paradoxical splitting: P2 occurs before A2 due to delayed aortic valve closure (left bundle branch blocker or aortic stenosis)
what type of valve defect is associated with a pulsatile liver and frog sign? why?
tricuspid regurgitation: reflux of blood during RV systole causes increase in jugular venous pressure (frog sign - distended jugular vein)
due to reflux through IVC, pulsatile liver can occur (liver pulsations can be palpated)
what is the origin of electrical impulse when you are looking at a narrow vs a wide QRS complex?
narrow QRS = conduction through fast conducting fibers (AV node, bundle, branches, Purkinje)
wide QRS = conduction through slower ventricular myocardium
how would you describe the pattern of rhythm seen in A-fib?
irregularly irregular !!!
basically no patterns
describe the vagomimetic effects of digitalis (digoxin)
digitalis: used to treat congestive heart failure (CHF) and atrial arrhythmias
increases inotropy (force of contraction), but also has vagomimetic (read: vagal nerve, PSNS) effects —> increases nodal delay to decrease HR
overall effect: stronger heart contractions but slower heart rate
how does hypocalcemia and hyperkalemia appear on an ECG, respectively?
hyper/hypocalcemia cause depolarization anomalies, while hyper/hypokalemia cause repolarization anomalies
hypocalcemia on ECG produces prolonged QT interval (shorter ventricular depolarization)
hyperkalemia on ECG produces tented T waves (longer repolarization)
where on an ECG do the following events occur?
a. activation of HCN channels
b. max ventricular myocyte calcium influx
c. SA node repolarization
d. Phase 1 of ventricular AP
e. AV nodal delay
f. plateau phase of ventricular AP
g. max ventricular myocyte sodium influx
a. activation of HCN channels: right before P wave (SA nodal AP)
b. max ventricular myocyte calcium influx: right after QRS, before T (plateau phase)
c. SA node repolarization: peak of P wave
d. Phase 1 of ventricular AP: beginning of downslope of QRS wave (transient hyperpolarization)
e. AV nodal delay: P-R interval
f. plateau phase of ventricular AP: right after QRS, before T (max calcium influx)
g. max ventricular myocyte sodium influx: peak of QRS complex
